The dorsal lateral geniculate nucleus (dLGN), the major thalamic station of the visual pathway, contains a fairly large number of dopaminergic terminals, and dopamine was found to reduce spontaneous and visually evoked activity in the dLGN in vivo. The cellular basis of this influence remained unknown. Here we have used whole cell patch-clamp techniques to analyse the effects of dopamine (DA) on GABAergic transmission in dLGN slices of juvenile postnatal day (P) 12-P24 Long-Evans rats or juvenile (P12-P22) GAD67-GFP (Deltaneo) mice. Spontaneous inhibitory postsynaptic currents (sIPSCs) were increased in frequency by the D(2)-like agonist quinpirole (QUIN) in rat (n = 6), as well as in mouse (n = 5) thalamic slices. This effect was blocked in the presence of the D(2)-like antagonist sulpiride (SULP, n = 5) and was absent in the ventrobasal complex (VB) of rat (n = 7) and mouse (n = 4) thalamus, which is devoid of GABAergic interneurons. Direct recordings from labelled GABAergic neurons in the dLGN of GAD67-GFP mice revealed a QUIN-mediated membrane depolarization (n = 12), which was attenuated by SULP (n = 6). These data demonstrate that DA through activation of D(2)-like receptors in GABAergic interneurons induces an increase in inhibitory interactions most likely at F2 dendrodendritic terminals, thereby providing a cellular correlate of the observation made in vivo that DA predominantly acts through inhibition of relay cell activity in the dLGN.